Apnea is a disorder characterized by temporary, recurrent interruptions of respiration. With apnea, respiration may cease completely for a minute or longer. One common form of apnea is sleep apnea, in which individual episodes of apnea can occur hundreds of times during a single night. Accordingly, patients with sleep apnea experience periodic wakefulness at night and excessive sleepiness during the day. In addition, apnea can exacerbate various medical conditions, particularly congestive heart failure (CHF) wherein the patient suffers from poor cardiac function. Other medical conditions that can be adversely affected by sleep apnea include: high blood pressure, risk for heart attack and stroke, memory problems, impotency and sexual dysfunction, migraine headaches, depression and anxiety, polycythemia (increase in the number of red blood cells), cor pulmonale (enlarged left ventricle of the heart), bradycardia (excessively slow heart rate), tachycardia (excessively fast heart rate), pulmonary hypertension hypoxemia (chronic daytime low blood oxygen) and hypercapnia (increased blood carbon dioxide (CO2)).
One form of sleep apnea is central sleep apnea (CSA), which is believed to be the result of a neurological condition. Briefly, respiration is regulated by groups of nerve cells in the brain in response to changing blood chemistry levels, particularly blood CO2 levels. When blood CO2 levels exceed a certain threshold, the groups of nerve cells generate a burst of nerve signals for triggering inspiration. The inspiration nerve signals are relayed via phrenic nerves to the diaphragm and via other nerves to chest wall muscles, which collectively contract to expand the lungs. With CSA, the nerve signals are not properly generated during extended periods of time while the patient is asleep or are of insufficient magnitude to trigger sufficient muscle contraction to achieve inhalation. In either case, the patient thereby fails to inhale until appropriate inspiration nerve signals are eventually generated—often not until after the patient awakes in response to significantly high blood CO2 levels. Arousal from sleep due to CSA usually lasts only a few seconds, but such brief arousals nevertheless disrupt continuous sleep leading to excessive sleepiness during the day, which diminishes quality of life. Excessive sleepiness during the day also increases risks due to accidents, particularly automobile accidents caused by the driver falling asleep due to the excessive daytime sleepiness. In addition, as already noted, frequent periods of apnea can exacerbate other medical conditions. In particular, aberrant blood chemistry levels occurring by sleep apnea are a significant problem for patients with CHF. Due to poor cardiac function caused by CHF, patients already suffer from generally low blood oxygen levels. Frequent periods of sleep apnea result in even lower blood oxygen levels. Fortunately, CSA is rare.
Another form of sleep apnea, which is more common, is obstructive sleep apnea (OSA) wherein the respiratory airway is temporarily blocked. With OSA, proper inspiratory nerve signals are generated by the brain and so the diaphragm and chest muscles contract in an attempt to cause the lungs to inhale. However, an obstruction of the upper respiratory airway blocks delivery of air to the lungs and so blood CO2 levels continue to increase, usually until the patient awakens and adjusts his or her position so as to reopen the obstructed respiratory airway so that normal breathing can resume. The site of obstruction is usually the soft palate, near the base of the tongue, which lacks rigid structures such as bone or cartilage for keeping the airway open. While the patient is awake, muscles near the soft palate keep the passage open. However, while asleep, the muscles can relax to a point where the airway collapses and hence becomes obstructed. As with CSA, arousal from sleep usually lasts only a few seconds but is sufficient to disrupt continuous sleep and prevent proper REM sleep.
Apnea can also occur during Cheyne-Stokes Respiration (CSR), which is an abnormal respiratory pattern often occurring in patients with CHF. CSR is characterized by alternating periods of hypopnea (i.e. reduced breathing) and hyperpnea (i.e. fast, deep breathing.) Briefly, CSR arises principally due to a time lag between blood CO2 levels sensed by the respiratory control nerve centers of the brain and the blood CO2 levels. With CHF, poor cardiac function results in poor blood flow to the brain such that the respiratory control nerve centers respond to blood CO2 levels that are no longer properly representative of the overall blood CO2 levels in the body. Hence, the respiratory control nerve centers trigger an increase in the depth and frequency of breathing in an attempt to compensate for perceived high blood CO2 levels—although the blood CO2 levels have already dropped. By the time the respiratory control nerve centers detect the drop in blood CO2 levels and act to slow respiration, the blood CO2 levels have already increased. This cycle becomes increasingly unbalanced until respiration alternates between hypopnea and hyperpnea. The periods of hypopnea often become sufficiently severe that no breathing occurs between the periods of hyperpnea, i.e. periods of frank apnea occur between the periods of hyperpnea. The wildly fluctuating blood chemistry levels caused by alternating between hyperpnea and apnea can exacerbate CHF and other medical conditions. Moreover, CSR can prevent the patient from achieving rapid eye movement (REM) sleep, which is needed. In this regard, REM sleep does not usually occur until after some period of the sustained Stage 3/Stage 4 sleep. CSR usually arises during Stage 3 sleep. Hence, repeated sleep interruptions occurring during CSR typically prevent the patient from achieving any REM sleep or, at least, an insufficient amount of REM sleep is achieved over the course of the night. When CHF is still mild, CSR usually occurs, if at all, only while the patient is sleeping. When it becomes more severe, CSR can occur while the patient is awake. Accordingly, CSR is one mechanism by which apnea can occur within patients who are awake.
In view of the significant adverse consequences of apnea, particularly insofar as patients with CHF are concerned, it is highly desirable to provide techniques for detecting and treating the condition. Apnea arising due to CSR is usually treated by addressing the source of the CSR, such as an underlying CHF. By reducing CHF so as to improve stroke volume, CSR is less likely to occur and so any periods of apnea arising during CSR may be avoided. OSA is usually treated by having the patient wear a breathing apparatus at night, such as a device providing continuous positive airway pressure (CPAP) therapy or bi-level positive pressure therapy (Bi-PAP). Surgery, however, is sometimes necessary. Although the source of CSA appears to be neurological, breathing devices employing CPAP or B-PAP techniques have been found to be effective for treating CSA as well. Although such breathing devices are effective when properly employed, they are often uncomfortable and inconvenient for the patient and, as a result, many patients fail to wear the device each night and hence forfeit the benefits thereof. In addition, when properly worn, the devices apply therapy continuously—even on nights when the patient might not have any actual episodes of sleep apnea.
Thus, many of these forms of therapy are delivered more or less continuously, at least while the patient is asleep, even when no episodes of apnea are occurring. In many cases, it would instead be desirable to automatically detect individual episodes of apnea and deliver therapy only as needed. In particular, it would desirable to provide such capability within an implantable medical system. Properly equipped, an implantable medical system could detect the onset of individual episodes of apnea and deliver appropriate therapy based upon the type of apnea. If an episode of non-obstructive apnea is detected, the device could then deliver periodic stimulation signals to the diaphragm via direct electrical stimulation of the phrenic nerves to cause the diaphragm to resume a proper respiratory rhythm. Within implantable systems lacking nerve stimulators for directly terminating the episode of apnea, warning signals may instead be generated (either via an implanted warning device or a bedside monitor) for awakening or otherwise alerting the patient so as to cause the patient to resume normal breathing. In any case, by promptly detecting the onset of an individual episode of apnea, therapy or warning signals can be promptly initiated so as to provide for prompt termination of the episode of apnea, thus reducing its adverse effects. Such as implantable medical system could utilize a pacemaker or ICD for use as a controller to coordinate the detection of episodes of apnea and the delivery of therapy in response thereto. Pacemakers and ICDs are usually implanted primarily for use in applying cardiac therapy for treating cardiac arrhythmias. However, many patients who are candidates for pacemakers or ICDs also suffer from apnea and hence could benefit from additional functionality directed to the detection and treatment of apnea.
Hence, it would be highly beneficial to provide techniques for detecting the onset of individual episodes of apnea, particularly for use within implantable medical systems. Heretofore, however, prompt and reliable detection of the onset of individual episodes of apnea has proven to be problematic. Even in the absence of apnea, respiration is often fairly infrequent (particularly while a patient is asleep) and so the lack of respiration for some period of time does not necessarily indicate the onset of apnea. False detection of apnea, when a patient is otherwise breathing properly, can result in unnecessary or improper therapy. Accordingly, to avoid such false positives, many conventional automatic apnea detection techniques require that no respiration be detected for some extended period of time—often twenty seconds or more—before an indication of apnea is made. By then, however, if apnea is indeed occurring, it has already been ongoing for some time and so prompt detection is not achieved.
Accordingly, it would be highly desirable to provide techniques for providing for faster detection of the onset of an individual episode of apnea and it is to this end that the invention is primarily directed. More specifically, the invention is primarily directed to detecting non-obstructive forms of apnea, such as CSA and apnea arising due to CSR.